The time was June 2000. Scientists with the Celera Genomics Corporation, in conjunction with the international Human Genome Project, announced that they had successfully derived the entire sequence of the human genome. Furthermore, they noted that humans share 99.9% of their genetic code with one another. This discovery served as the platform for the medical community to declare that there was no genetic foundation for the notion of race, and we were all just human beings.

The problem with this assertion is that the human genome is comprised of over 3 billion base pairs. Therefore, a 0.1% difference between individuals amounts to 3 million base pairs. A mutation in a single base pair can mean the difference between having a disease and not having a disease, as in the case of thalassemia, cystic fibrosis, muscular dystrophy, or hemophilia. One can easily see that 3 million is far from insignificant in terms of differentiating who we are. If nuclear families are closely related genetically, and are more prone to certain diseases, why wouldn’t groups of people with common ancestral lines share this same propensity?

Interestingly, in September 1999, right around the same time as the Human Genome Project a retrospective study was published in the Journal of Cardiac Failure by Carson et al titled, “Racial differences in response to therapy for heart failure: Analysis of the vasodilator-heart failure trials.” In this study, they analyzed data from two previous trials studying the use of ACE inhibitors, isosorbide, and hydralazine in the treatment of congestive heart failure. When the data was split apart by race, there was a statistically significant decrease in the response of African American patients to the drug enalapril, and a statistically significant decrease in the effectiveness of hydralazine/isosorbide in white patients. The conclusion of the analysis was that certain drugs respond better for some races than others. In response to this study, the drug carvediol was studied specifically in the African American and white populations to say conclusively that it benefited both groups equally, and this became a marketing point for the pharmaceutical company that manufactures carvediol.

Should race play a factor in treating hypertension? According to the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which is the gold standard for treatment, the answer is yes. The end of the report includes a section on “special considerations” in medication selection, and suggests a different course for African American patients or other minorities as opposed to white patients. The implications of this recommendation are obvious. If the medical profession is willing to admit that there are biochemical differences between races, then the ethical line in the sand regarding racial profiling and has been blurred. While the role of racial considerations in medicine is undoubtedly a controversial one, make no mistake that doctors are being advised to treat differently based on race.

References

P CARSON, S ZIESCHE, G JOHNSON, J COHN, FORTHEVASODILATORHEARTFAILURE (1999). Racial differences in response to therapy for heart failure: Analysis of the vasodilator-heart failure trials1, 2 Journal of Cardiac Failure, 5 (3), 178-187 DOI: 10.1016/S1071-9164(99)90001-5

A. V. Chobanian (2003). Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Hypertension, 42 (6), 1206-1252 DOI: 10.1161/01.HYP.0000107251.49515.c2

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